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首页> 外文期刊>Science Advances >Global increase in replication fork speed during a p57KIP2-regulated erythroid cell fate switch
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Global increase in replication fork speed during a p57KIP2-regulated erythroid cell fate switch

机译：在p57 KIP2 调节的类红细胞命运切换期间复制叉速度的整体提高

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Cell cycle regulators are increasingly implicated in cell fate decisions, such as the acquisition or loss of pluripotency and self-renewal potential. The cell cycle mechanisms that regulate these cell fate decisions are largely unknown. We studied an S phase–dependent cell fate switch, in which murine early erythroid progenitors transition in vivo from a self-renewal state into a phase of active erythroid gene transcription and concurrent maturational cell divisions. We found that progenitors are dependent on p57KIP2-mediated slowing of replication forks for self-renewal, a novel function for cyclin-dependent kinase inhibitors. The switch to differentiation entails rapid down-regulation of p57KIP2 with a consequent global increase in replication fork speed and an abruptly shorter S phase. Our work suggests that cell cycles with specialized global DNA replication dynamics are integral to the maintenance of specific cell states and to cell fate decisions.
机译：细胞周期调节剂越来越多地参与细胞命运的决定，例如多能性的获得或丧失以及自我更新的潜力。调节这些细胞命运决定的细胞周期机制在很大程度上是未知的。我们研究了S期依赖的细胞命运转换，其中鼠类早期类红细胞祖细胞在体内从自我更新状态过渡到活性类红细胞基因转录和同时成熟细胞分裂的阶段。我们发现祖细胞依赖于p57 KIP2 介导的复制叉减慢自我更新，这是细胞周期蛋白依赖性激酶抑制剂的一种新功能。转向差异化意味着p57 KIP2 的快速下调，随之而来的是复制叉速度的整体提高和S期的突然缩短。我们的工作表明，具有专门的全局DNA复制动力学的细胞周期对于维持特定细胞状态和决定细胞命运至关重要。

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